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Human Monoclonal CACNG2 Primary Antibody for ICC, IF - ABIN1686631
Khodosevich, Jacobi, Farrow, Schulmann, Rusu, Zhang, Sprengel, Monyer, von Engelhardt: Coexpressed auxiliary subunits exhibit distinct modulatory profiles on AMPA receptor function. in Neuron 2014
Mouse (Murine) Polyclonal CACNG2 Primary Antibody for WB - ABIN2476592
Gibbons, Houte: Bacterial adherence in oral microbial ecology. in Annual review of microbiology 1975
Show all 2 Pubmed References
Study shows the expression of the TARP (show TARP Antibodies) gamma2 in a non-mammalian vertebrate, and reveals a functional role for Cacng2a in synaptic physiology and development; suggests that Cacng2a is required for normal trafficking and function of synaptic AMPARs, while Cacng2b is largely non-functional with respect to the development of AMPA (show GRIA3 Antibodies) synaptic transmission
The results from the current study demonstrate that there is an aberrant tissue expression of GABAAR (show GABRG2 Antibodies) alpha1 and beta2 subunits in the thalamus of PN7-9 juvenile stargazer mice, but that this early change equilibrates during later developmental stages (PN10-12 and PN13-15).
Critically, by altering the two interacting loops of TARP (show TINAGL1 Antibodies) gamma2 and TARP (show TINAGL1 Antibodies) gamma8, the authors could entirely remove all allosteric modulation of GluA2 (show GRIA2 Antibodies), without affecting formation of AMPA (show GRIA3 Antibodies) receptor-TARP (show TINAGL1 Antibodies) complexes.
Learning to cope with stress modulates anterior cingulate cortex stargazin expression in mice.
show that upon release of glutamate (show GRIN1 Antibodies), synaptic AMPARs were desensitized by transmitter by >90%. As glutamate (show GRIN1 Antibodies) levels subsequently fell, recovery of transmission occurred due to the presence of the AMPAR accessory protein stargazin that enhances the AMPAR response to low levels of transmitter.
we show that the TARP gamma-2 (stargazin) is present in spinal dorasl horn neurons and is necessary in a form of inflammatory pain-induced plasticity
the density of AMPARs correlates with that of TARP gamma-2 across SCC (show CYP11A1 Antibodies) synapses and its high expression is linked to high-density AMPAR expression at perforated type of pyramidal cell synapses
in the absence of stargazin, the refinement of the retinogeniculate synapse is specifically disrupted during the experience-dependent phase. Stargazin expression and phosphorylation increased with visual deprivation.
SR interacts with the synaptic proteins, postsynaptic density protein 95 (PSD-95 (show DLG4 Antibodies)) and stargazin, forming a ternary complex.
Region-specific differences investigated in GABAA (show GABRg1 Antibodies) receptor (GABAAR (show GABRG2 Antibodies)) subunit expression occur in the ventral posterior and reticular thalamic nucleus regions in the stargazer mouse model of absence epilepsy.
The combined loss of the AMPA (show GRIA3 Antibodies) receptor auxiliary TARPg-2 subunit and the GluK5 (show GRIK1 Antibodies) subunit leads to early mouse lethality.
TARP gamma-2 reduces the ability of low glutamate (show GRIN1 Antibodies) concentrations to cause AMPAR desensitization and enhances channel gating at low glutamate (show GRIN1 Antibodies) occupancy.
Our nanopositioning data place stargazin below the AMPA (show GRIA3 Antibodies) receptor ligand-binding domain, where it is well poised to act as a scaffold to facilitate the long-range conformational selection observations seen in single-molecule experiments. These data support a model of stargazin acting to stabilize or select conformational states that favor activation.
In addition to changes in MEK3 (show MAP2K3 Antibodies) gene regulation, our study demonstrated upregulation of CACNG2 and GADD45G (show GADD45G Antibodies) at the mRNA level in CMM patients.
A transient positive feedback mechanism between AMPAR and stargazin has implications for information processing in the brain, because it should allow activity-dependent facilitation of excitatory synaptic transmission through a postsynaptic mechanism.
The additional cleft closure and/or stabilization of the more closed-cleft states of the LBD is expected to translate to higher agonist efficacy and could contribute to the structural mechanism for stargazin modulation of AMPAR function.
Autoinactivation is a subunit and splice form dependent property of AMPA (show GRIA3 Antibodies) receptor-stargazin complexes, which involves structural rearrangements within the complex rather than any physical dissociation.
Susceptibility to chronic pain following nerve injury is genetically affected by CACNG2
examined distribution of the stargazin-like proteins gamma2, gamma3, and gamma4 in human CNS: gamma2 is expressed in cerebellum, cerebral cortex, hippocampus and thalamus, whereas gamma3 abounds in cerebral cortex & amygdala and gamma4 in basal ganglia
These results suggest that stargazin (gamma-2) not only promotes AMPA (show GRIA3 Antibodies) receptor surface expression but also directly modulates AMPA (show GRIA3 Antibodies) receptor activity.
AMPA (show GRIA3 Antibodies) receptors complexed with stargazin are significantly more responsive to synaptically released glutamate (show GRIN1 Antibodies) compared with AMPA (show GRIA3 Antibodies) receptors lacking stargazin.
The protein encoded by this gene is a type I transmembrane AMPA receptor regulatory protein (TARP). TARPs regulate both trafficking and channel gating of the AMPA receptors. This gene is part of a functionally diverse eight-member protein subfamily of the PMP-22/EMP/MP20 family. This gene is a susceptibility locus for schizophrenia.
voltage-dependent calcium channel gamma-2 subunit
, calcium channel, voltage-dependent, gamma subunit 2
, TARP gamma 2
, TARP gamma-2
, neuronal voltage-gated calcium channel gamma-2 subunit
, transmembrane AMPAR regulatory protein gamma-2